http://purl.uniprot.org/citations/37393064 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/37393064 | http://www.w3.org/2000/01/rdf-schema#comment | "PurposeWe hypothesized that Transforming growth factor beta receptor 2 (Tgfbr2) deletion in keratocyte (Tgfbr2kera-cko), the corneal stroma cell, can result in corneal thinning and generate a potential model for Cornea Ectasia (CE).MethodsCorneal thickness of Tgfbr2kera-cko and Tgfbr2Ctrl was examined with Optical Coherence Tomography (OCT) at post-natal (P) days 42 and 70, respectively. Histological H&E staining, transmission electron micrograph (TEM), and immunofluorescence staining (IFS) were harnessed to examine corneal cell morphology, proliferation, differentiation, and collagen fibrils.ResultsSlit-Lamp revealed that corneas were transparent in both Tgfbr2kera-cko and Tgfbr2Ctrl, however, Tgfbr2kera-cko cornea was 33.5% and 42.9% thinner as compared with those of Tgfbr2Ctrl at P42 and P70, respectively. H&E and semithin section staining with toluidine blue-O confirmed that Tgfbr2kera-cko cornea has a thinner stroma. In contrast, the epithelium in Tgfbr2kera-cko was substantially thicker. The cell proliferation marker Ki67 expression level increased ∼9% in Tgfbr2kera-cko corneal epithelium as compared with that in Tgfbr2Ctrl, however, the Krt14 and Krt12 expression pattern was not obviously changed in Tgfbr2kera-cko corneal epithelium. It was noticed that Col1a1 expression was substantially reduced in Tgfbr2kera-cko as compared with that in Tgfbr2Ctrl. TEM showed that keratocytes were unhealthy and stromal collagen fibril density was significantly reduced in Tgfbr2kera-cko as compared with that in Tgfbr2Ctrl cornea. Moreover, mechanical eye-rubbing on Tgfbr2kera-cko resulted in corneal hydrops and edema.ConclusionTgfbr2 in keratocytes is indispensable for the corneal stroma at postnatal homeostasis. The cornea phenotype manifested in these Tgfbr2kera-cko mice resembles corneal ectasia disease in humans."xsd:string |
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http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/author | "Liu C.Y."xsd:string |
http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/author | "Yuan Y."xsd:string |
http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/author | "Wang Y.C."xsd:string |
http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/author | "Kao W."xsd:string |
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http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/author | "Yeh L.K."xsd:string |
http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/author | "Yasoda S."xsd:string |
http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/author | "Zolnik O.B."xsd:string |
http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
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http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/title | "Transforming growth factor beta receptor 2 (Tgfbr2) deficiency in keratocytes results in corneal ectasia."xsd:string |
http://purl.uniprot.org/citations/37393064 | http://purl.uniprot.org/core/volume | "29"xsd:string |
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